参芍片对大鼠心肌缺血再灌注损伤的保护作用

Protective effects of Shenshao Tablets on myocardial ischemia-reperfusion injury in rats

目的探讨参芍片对大鼠急性心肌缺血再灌注(MI/R)的保护作用。方法采用经典冠状动脉左前降支结扎再灌注手术构建MI/R损伤模型。40只大鼠随机分为假手术组,模型组,参芍片组(1.87g/kg)和阿托伐他汀阳性药物组(80mg/kg),每组8只,灌胃给药1次/d,连续7d。记录大鼠心脏血流动力学指标,TTC染色法测定大鼠心肌梗死范围,HE染色和TUNEL染色法分别观察心肌组织形态学和心肌细胞凋亡,生化法测定LDH、CK MB、SOD、MDA、GSH Px水平,ELISA法测定血清TNFα、IL 1β水平,Western blot法检测大鼠心肌组织Bax、Bcl 2蛋白表达。结果与模型组比较,参芍片组心肌梗死范围明显减小(P<0.01),改善血流动力学指标、心肌病理性状态以及心肌细胞凋亡,血清中LDH、CK MB、MDA、TNFα、IL 1β水平明显降低(P<0.05,P<0.01),而血清SOD、GSH Px水平则显著升高(P<0.05),明显降低了大鼠心肌组织Bax/Bcl 2比例(P<0.01)。结论参芍片能减少大鼠MI/R引起的心肌损伤、氧化损伤、炎症反应和关键凋亡蛋白表达,从而对心血管起保护作用。

AIM To investigate the protective effects of Shenshao Tablets(SST)on myocardial ischemia reperfusion(MI/R)injuryinrats.METHODS TheMI/Rinjurymodelwasproducedbyusingtheligationofthe left anterior descending coronary artery.Forty rats were randomly divided into sham operation group,model group,SSTgroup(187g/kg)andatorvastatinpositivedruggroup(80mg/kg),withtenratsineachgroupfortreatment once a day by gavage for 7 consecutive days.The rats had their hemodynamic parameters of hearts recorded,their myocardial infarct size determined by TTC staining,and their myocardial histomorphology and cardiomyocyte apop tosis observed by HE staining and TUNEL staining,respectively.Their levels of LDH,CK MB,SOD,MDA,and GSH Px were determined by biochemical method,their levels of serum TNFαand IL 1βwere measured by ELISA,and finally their expressions of myocardiac Bax and Bcl 2 were detected by Western blot.RESULTS Compared with the model group,the SST group shared significantly reduced myocardial infarction range(P<001),improved hemodynamic parameters,myocardial pathological state and myocardial apoptosis,significantly decreasedserumLDH,CK MB,MDA,TNFα,IL 1βlevels(P<0.05,P<0.01),significantlyincreasedserum SODandGSH Pxlevels(P<0.05),andsignificantlyreducedBax/Bcl 2proportioninratmyocardialtissue(P<0.01).CONCLUSION Being a significant protector of the rats’cardiovascular functions,SST limits the myo cardial injury,the oxidative damages,the inflammatory reactions,and the key apoptotic protein expressions.